Gorzelniak Kerstin, Engeli Stefan, Janke Jürgen, Luft Friedrich C, Sharma Arya M
Helios Klinkum Berlin, Franz Volhard Clinic - Charité and Max Delbrück Center for Molecular Medicine, Humboldt University of Berlin, Germany.
J Hypertens. 2002 May;20(5):965-73. doi: 10.1097/00004872-200205000-00032.
Adipose tissue secretes vasoactive substances which may contribute to the development of obesity-related hypertension. The aim of this work was to study the expression of renin-angiotensin system genes in adipose tissue of obese hypertensive subjects and the hormonal regulation of these genes.
Differential expression of renin-angiotensin system genes in subcutaneous abdominal adipocytes of 12 lean normotensive, eight obese normotensive, and 10 obese hypertensive women was determined in a cross-sectional study. In vitro hormonal regulation of these genes was studied in primary human adipocytes obtained by breast reduction from healthy women.
In the clinical study, 24-h ambulatory blood pressure measurement and anthropometry were used to characterize the volunteers, and adipocytes were obtained by subcutaneous needle biopsy. The in vitro regulation of renin-angiotensin system genes by hydrocortisone, insulin, thyroxin, estradiol and angiotensin II on primary cultured human mammary adipocytes was studied by quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
While expression of the angiotensinogen gene was significantly lower in adipocytes from both obese groups, the renin, angiotensin-converting enzyme and angiotensin II type 1 receptor genes were significantly upregulated in obese hypertensives. Hydrocortisone increased angiotensin II type 1 receptor gene and protein expression in a time- and dose-dependent manner in human adipocytes, but had no significant influence on other renin-angiotensin system genes. Expression of these genes was not significantly affected by any of the other tested hormones.
Renin-angiotensin system genes are differentially regulated in human obesity and hypertension. The role of the adipose-tissue renin-angiotensin system in the development of obesity-associated hypertension or metabolic disease clearly warrants further study.
脂肪组织分泌血管活性物质，这可能促成与肥胖相关的高血压的发展。本研究的目的是探讨肥胖高血压患者脂肪组织中肾素 - 血管紧张素系统基因的表达以及这些基因的激素调节。
在一项横断面研究中，测定了12名瘦的血压正常、8名肥胖血压正常和10名肥胖高血压女性的腹部皮下脂肪细胞中肾素 - 血管紧张素系统基因的差异表达。在通过对健康女性进行缩乳手术获得的原代人脂肪细胞中研究了这些基因的体外激素调节。
在临床研究中，使用24小时动态血压测量和人体测量学对志愿者进行特征描述，并通过皮下针吸活检获取脂肪细胞。通过定量逆转录聚合酶链反应（RT-PCR）研究氢化可的松、胰岛素、甲状腺素、雌二醇和血管紧张素II对原代培养的人乳腺脂肪细胞中肾素 - 血管紧张素系统基因的体外调节。
虽然两个肥胖组的脂肪细胞中血管紧张素原基因的表达均显著降低，但肥胖高血压患者的肾素、血管紧张素转换酶和血管紧张素II 1型受体基因显著上调。氢化可的松在人脂肪细胞中以时间和剂量依赖性方式增加血管紧张素II 1型受体基因和蛋白表达，但对其他肾素 - 血管紧张素系统基因没有显著影响。这些基因的表达不受任何其他测试激素的显著影响。
肾素 - 血管紧张素系统基因在人类肥胖和高血压中受到不同调节。脂肪组织肾素 - 血管紧张素系统在肥胖相关高血压或代谢疾病发展中的作用显然值得进一步研究。
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